Role of cyclooxygenase‐2 in the control of renal haemodynamics and excretory function

López, Ruth M.; Roig, Francisco J.; Llinás, María T.; Salazar, Francisco

doi:10.1046/j.1365-201x.2003.01103.x

Cited by 20 publications

(17 citation statements)

References 38 publications

(82 reference statements)

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“…Specifically, the high constitutive expression of COX2 in killifish gills, opercular epithelia and kidney suggest a role in regulating ion transport as has been shown in mammalian kidneys (Harris and Breyer, 2001;López et al, 2003) and shark rectal glands (Yang et al, 2002). Expression of COX2 was also found to be highest in the gills of zebrafish (Grosser et al, 2002), suggesting that COX2 is constitutively expressed at high levels in the gills of all teleosts.…”

Section: Cox2 Distribution and Localization In Gillsmentioning

confidence: 86%

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Choe

Havird

Rose

et al. 2006

Journal of Experimental Biology

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SUMMARY In the kidneys of mammals, cyclooxygenase type 2 (COX2) is expressed in medullary interstitial cells, the macula densa and epithelial cells of the cortical thick ascending limb where it generates prostaglandins that regulate hormone secretion, inhibit ion transport, and support cell survival during salt loading and dehydration. In teleosts, the gills are in direct contact with an aquatic environment and are the dominant site of osmoregulation. During transfers between salinities, specialized cells in the gills (chloride cells) rapidly regulate NaCl secretion for systemic osmoregulation while they simultaneously are exposed to acute osmotic shock. This study was conducted to determine if COX2 is expressed in the gills, and if so, to evaluate its function in cellular and systemic osmoregulation. Degenerate primers, reverse transcription–PCR and rapid amplification of cDNA ends were used to deduce the complete cDNA sequence of a putative COX2 enzyme from the gills of the euryhaline killifish (Fundulus heteroclitus). The 2738 base pair cDNA includes a coding region for a 610 amino acid protein that is over 70%identical to mammalian COX2. A purified antibody generated against a conserved region of mouse COX2 labeled chloride cells, suggesting that the enzyme may control NaCl secretion as an autocrine agent. Real-time PCR was then used to demonstrate that mRNA expression of the COX2 homologue was threefold greater in gills from chronic seawater killifish than in gills from chronic freshwater killifish. Expression of Na+/K+/2Cl–cotransporter and the cystic fibrosis transmembrane conductance regulator were also greater in seawater, suggesting that chronic COX2 expression in the gills is regulated in parallel to the key ion transporters that mediate NaCl secretion. Real-time PCR was also used to demonstrate that acute transfer from seawater to freshwater and from freshwater to seawater led to rapid, transient inductions of COX2 expression. Together with previous physiological evidence,the present molecular and immunological data suggest that constitutive branchial COX2 expression is enhanced in seawater, where prostaglandins can regulate NaCl secretion in chloride cells. Our data also suggest that branchial COX2 expression may play a role in cell survival during acute osmotic shock.

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Section: Cox2 Distribution and Localization In Gillsmentioning

confidence: 86%

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Choe

Havird

Rose

et al. 2006

Journal of Experimental Biology

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“…The prostaglandins perform a homeostatic role within the normal and compromised kidney Imig 2000) and are generated by two isoforms of the enzyme-converting arachidonic acid: cyclooxygenase-1 (COX-1) and COX-2. COX-2 has been found to be constitutively active within the kidney, expressed in pre-and post-glomerular endothelium (Therland et al 2004), and important in normal kidney hemodynamic function (Lopez et al 2003). There are a number of studies that suggest a relationship between NO and COX systems in the regulation of vascular tone Harris et al 2000).…”

Section: Discussionmentioning

confidence: 98%

Glutamine contributes to ameliorate inflammation after renal ischemia/reperfusion injury in rats

Esposito

Mondello

Paola

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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The aim of this study was to investigate the effects of glutamine in an in vivo rat model of renal ischemia/reperfusion (I/R) injury. Male Wistar rats underwent bilateral renal pedicle clamping for 45 min followed by reperfusion for 6 h. Glutamine (1.5 mg/kg) was administered intraperitoneally (i.p.) 15 min prior to reperfusion. Plasma concentrations of urea, creatinine, γ-glutamyl transferase (γ-GT), and aspartate aminotransferase (AST) were measured for the assessment of renal function and reperfusion injury. Markers of oxidative stress, expression of the pro-inflammatory mediators inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), AT-1 expression, and changes in the oxidative stress-sensitive nuclear factor kappa B (NF-κB) signaling pathway were measured to investigate whether glutamine can reduce the renal dysfunction. Kidney myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels were measured for assessment of polymorphonuclear (PMN) cell infiltration and lipid peroxidation, respectively. Renal sections were used for histologic grading of renal injury and for immunohistochemical localization of nitrotyrosine and poly(ADP-ribose) synthetase (PARS). In vivo, glutamine significantly reduced the increase in urea, creatinine, γ-GT, AST, produced by renal ischemia/reperfusion (I/R), suggesting an improvement in both renal function and injury. Glutamine significantly reduced iNOS and NF-κB, kidney MPO activity and MDA levels, indicating a reduction in PMN infiltration and lipid peroxidation, respectively. Glutamine reduced the histological evidence of renal damage associated with I/R and caused a substantial reduction in the staining for nitrotyrosine and PARS, suggesting reduced nitrosative and oxidative stress. Moreover, glutamine attenuated the reduction of COX-2 expression and prevented the increased AT-1 expression after I/R. Our results suggest that glutamine reduces the renal dysfunction and injury associated with I/R of the kidney.

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“…Since nitric oxide (NO) regulates renal cortical COX-2 expression [28], Lopez et al [29] proposed that in addition to the salt depletion and prolonged duration of COX-2 inhibition, reduced NO may be another factor underlying these effects of COX-2-specific inhibitors on renal hemodynamic.…”

Section: Discussionmentioning

confidence: 99%

Cardiorenal Effects of Newer NSAIDs (Celecoxib) versus Classic NSAIDs (Ibuprofen) in Patients with Arthritis

Hegazy

Alashhab

Amin

2011

Journal of Toxicology

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Background. Arthritis is a common condition that co-exists in the elderly population. This condition leads to frequent administration of comorbid analgesics especially non steroidal anti-inflammatory drugs (NSAIDs). Aim. To study cardiorenal toxicity of celecoxib versus ibuprofen in arthritic patients. Subjects and Methods. Seven hundred ninety-wo arthritic patients were enrolled in the study for 6 months. Three hundred ninety-six patients administered celecoxib 400 mg twice a day; 396 patients administered ibuprofen 300 mg three times a day. Effects measured included investigator-reported hypertension, edema, or congestive heart failure, increases in serum creatinine or reduction in serum creatinine clearance, and changes in serum electrolytes. Results. Celecoxib was associated with significant (P < .05) lower incidence of hypertension and edema in comparison with ibuprofen. Systolic hypertension occurred significantly less (P < .05) with celecoxib compared with ibuprofen. Serum creatinine was significantly increased (P < .05) in patients treated with ibuprofen in comparison with celecoxib. Creatinine clearance was significantly lower (P < .05) in cases treated with ibuprofen in comparison to celecoxib. Nonsignificant changes in serum body electrolytes occurred. Conclusion. The most important finding of this study was the lowering incidence of cardiorenal toxicity of celecoxib in comparison with ibuprofen.

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Role of cyclooxygenase‐2 in the control of renal haemodynamics and excretory function

Abstract: Contrary to the important role of COX-2 in the long-term regulation of renal haemodynamics, the metabolites derived from COX-2 seem to be only involved in the acute regulation of renal excretory function.

Cited by 20 publications

References 38 publications

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Glutamine contributes to ameliorate inflammation after renal ischemia/reperfusion injury in rats

Cardiorenal Effects of Newer NSAIDs (Celecoxib) versus Classic NSAIDs (Ibuprofen) in Patients with Arthritis

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